Panoply™ Human IL22 Knockdown Stable Cell Line

Reducing drug resistance in tumor cells has become a critical issue in cancer therapy. In this study, researchers investigated whether IL-22 contributes to paclitaxel (PTX) resistance in lung cancer cells and explored the underlying molecular mechanisms. The results showed that IL-22 expression was significantly higher in A549/PTX cells compared to A549 cells. Knockdown of the IL-22 gene significantly enhanced the inhibitory effect of PTX on A549/PTX cell proliferation and reduced the IC50 value of PTX for this cell line, indicating that IL-22 plays a role in PTX resistance. Furthermore, IL-22 knockdown significantly increased PTX-induced apoptosis in A549/PTX cells; concurrently, the expression levels of p-JNK and Caspase-3 were markedly elevated, while Bcl-2 expression was significantly reduced. These findings suggest that IL-22 contributes to PTX resistance in A549 cells by regulating apoptosis via the JNK signaling pathway.

To investigate the potential molecular mechanisms underlying IL-22-mediated cellular resistance to PTX, researchers evaluated the JNK signaling pathway. The results showed that IL-22 knockdown activated the JNK signaling pathway, evidenced by a significant increase in p-JNK expression in IL-22-knockdown A549/PTX cells. Furthermore, compared with the control and negative control groups, IL-22-knockdown A549/PTX cells exhibited significantly increased Caspase-3 expression and significantly decreased Bcl-2 expression (Figure 1).

Figure 1. IL-22 modulated JNK signaling pathway. (Li C, et al., 2018)